Respiratory difficulties

During the period December 1-5, 1930, an intense fog occupied the heavily industrialized Meuse Valley between Liege and Huy (about 24 km) in eastern Belgium (1). Several hundred persons had respiratory attacks primarily beginning on the 4th and 63 persons died on the 4th and 5th after a few hours of sickness. On December 6 the fog dissipated the respiratory difficulties improved and, in general, rapidly ceased. 

Monitoring and Managing Adverse Drug Reactions The nurse observes the patient at frequent intervals, especially during the first 48 hours of therapy. It is important to report to the primary health care provider the occurrence of any adverse reaction before the next dose of the drug is due The nurse should report serious adverse reactions, such as a severe hypersensitivity reaction, respiratory difficulty, severe diarrhea, or a decided drop in blood pressure, to the primary health care provider immediately because a serious adverse reaction may require emergency intervention. 

Neuromuscular blockade or respiratory paralysis may occur after administration of the aminoglycosides Therefore, it is extremely important that any symptoms of respiratory difficulty be reported immediately. If neuromuscular blockade occurs, it may be reversed by the administration of calcium salts but mechanical ventilation may be required. 

Promoting an Optimal Response to Therapy Monitoring each patient for response to drug therapy and for the appearance of adverse reactions is an integral part of promoting an optimal response to therapy. The nurse immediately reports serious adverse reactions, such as signs and symptoms of a hypersensitivity reaction or superinfection, respiratory difficulty, or a marked drop in blood pressure... 

The nurse should immediately report to the primary health care provider any significant changes in the blood pressure, the pulse rate or rhythm, respiratory difficulty, change in respiratory rate or rhythm, or change in the patient s general condition. 

Clinical features include neonatal hypotonia, a tendency toward congenital hip dislocation and diffuse muscle weakness. Later on children are frequently of short stature and low body weight and often have long thin faces and high-arched palates. Respiratory difficulties, where present, occur early on and tend to improve with time. In others a virtually static clinical picture is seen. 

Amphotericin B is the mainstay of treatment of patients with severe endemic fungal infections. The conventional deoxycholate formulation of the drug can be associated with substantial infusion-related adverse effects (e.g., chills, fever, nausea, rigors, and in rare cases hypotension, flushing, respiratory difficulty, and arrhythmias). Pre-medication with low doses of hydrocortisone, acetaminophen, nonsteroidal anti-inflammatory agents, and meperidine is common to reduce acute infusion-related reactions. Venous irritation associated with the drug can also lead to thrombophlebitis, hence central venous catheters are the preferred route of administration in patients receiving more than a week of therapy. 

Choline acetyltransferase deficiency. The distinguishing clinical feature is sudden episodes of severe respiratory difficulty and oropharyngeal (bulbar) weakness leading to apnea (cessation of respiration) precipitated by infections, fever or excitement, or occurring even spontaneously. In some patients, the disease presents at birth with hypotonia... 

It is clear that both the form of molybdenum administered and the route of exposure affect molybdenum metabolism and survival (Table 30.4). By comparison, adverse effects (some deaths) were noted at 250 mg Mo/kg body weight (BW) (in guinea pigs), at 50 mg/kg BW in domestic cats (central nervous system impairment), at 10 mg/L drinking water in mice (survival), at 10 to 15 mg total daily intake in humans (high incidence of gout-like disease), and at to 3 mg/m3 air in humans for 5 years (respiratory difficulties), or 6 to 19 mg/m3 in humans for 4 years (Table 30.4). 

Pruritus, jaundice, palmar erythema, spider angiomata, hyperpigmentation Gynecomastia, reduced libido Ascites, edema, pleural effusion, and respiratory difficulties Malaise, anorexia, and weight loss Encephalopathy Laboratory tests Hypoalbuminemia Elevated prothrombin time Thrombocytopenia Elevated alkaline phosphatase... 

Chemical identification of both gas- and particle-phase compounds occurring in the atmosphere that cause eye irritation and respiratory difficulties. 

Symptoms of exposure Exposure to vapors may cause lacrimation, nose, and throat irritation and respiratory difficulty. Oral intake or absorption through skin may produce asthma, chest pain, dyspnea, pulmonary edema, breathing difficulty, and death (Patnaik, 1992). An irritation concentration of 5.00 mg/m in air was reported by Ruth (1986). 

It is expected that severe exposure would produce a broad spectrum of clinical effects indicative of massive overstimulation of the cholinergic system including headache, weakness, dizziness, blurred vision, respiratory difficulty, paralysis, convulsions, and coma. 

Exposure of animals to 5 00 ppm caused immediate gasping, swelling of eyelids, corneal opacity, lacrimation, and excessive salivation. Levels of 100 ppm produced the same effects after 3 minutes 50 ppm for 30 minutes caused deaths. Chronic exposure above 3 ppm produced severe nephrosis, marked toxic hepatosis, and severe respiratory difficulty in some of the exposed animals. 

A 44-year-old male worker experienced a large skin area exposure to a mixture of CAC, benzene, and xylidine. The worker was put under a shower within 5 minutes of the accident, but shortly thereafter he began to have respiratory difficulties and experienced an apparent grand mal seizure. The patient was still comatose 2 years after the accident. Burns caused by the chloroacetyl chloride were believed to have enhanced skin absorption of the other two chemicals, although the relative contribution of the three chemicals to the... 

Repeated exposures to 250 ppm (twice for 4 hours) or 100 ppm (twelve 6-hour exposures) caused eye and nose irritation and respiratory difficulty in rats at autopsy, there was degeneration of renal tubules and injury to the adrenals. Fifteen exposures to 5 or 10 ppm resulted in no observed toxic effect, except for retarded weight gain at the higher dose. 

Accidental ingestion has caused fatalities effects were repeated, violent, clonic convulsions, sometimes superimposed on a continuous tonic spasm. Respiratory difficulty and cyanosis, secondary to the convulsions, were common. After nonfatal accidental ingestions, symptoms have included malaise, dizziness, nausea, and vomiting. Agitation, collapse, convulsions, loss of consciousness, muscle tremor, fever, and cyanosis have commonly been observed. Most patients who survive recover completely over 1-3 days protracted illness is... 

Administration of large doses of quinone to experimental animals caused local irritation, clonic convulsions, respiratory difficulties, drop in blood pressure, and death due to paralysis of the medullary centers. In chronic studies, quinone has been tested in mice by skin application and inhalation and in rats by subcutaneous injection. The lARC has determined that there is inadequate evidence in experimental animals for carcinogenicity of quinone and that it is not classifiable as to its carcinogenicity to humans. ... 

Disuifiram-aicohoi reaction Disulfiram plus alcohol, even small amounts, produces flushing, throbbing in head and neck, throbbing headaches, respiratory difficulty, nausea, copious vomiting, sweating, thirst, chest pain, palpitations, dyspnea, hyperventilation, tachycardia, hypotension, syncope, marked uneasiness, weakness, vertigo, blurred vision, and confusion. In severe reactions there may be respiratory depression, cardiovascular collapse, arrhythmias. Ml, acute CHF, unconsciousness, convulsions, and death. The intensity of the reaction is proportional to the amounts of disulfiram and alcohol ingested. The duration of the reaction varies from 30 to 60 minutes to several hours. 

Airway. Ensure a patent airway via endotracheal intubation or cricothyrotomy (ie, inferior laryngotomy, used prior to tracheotomy) and administer oxygen. Severe respiratory difficulty may respond to IV aminophylline or to other bronchodilators. Hypotension The patient should be recumbent with feet elevated. Depending upon the severity, consider the following measures ... 

Respiratory Effects. Respiratory rates were decreased in mice exposed to vapors of hexachlorobutadiene at concentrations of 155 ppm or greater for 15 minutes. The authors characterized the responses as a reaction to nasal irritation (de Ceaurriz et al. 1988). Nasal irritation and respiratory difficulty was also reported in rats exposed to vapors at a concentration of 250 ppm for 2 days (4 hours/day) or 100 ppm for 12 days (6 hours/day) (Gage 1970). Breathing difficulty occurred even with exposure to 25 ppm for 15 days (6 hours/day). 

Gastric lavage is contraindicated because of the serious danger of aspiration and the relatively benign gastrointestinal effects. Patients with respiratory difficulties require oxygen and sometimes mechanical ventilation. Pulmonary oedema, if it occurs, should be treated with diuretics (furosemide 25-100 mg intravenously) or by mechanical ventilation. Antibiotic treatment is unnecessary unless bacterial pneumonia, a rare sequel to kerosene pneumonitis, develops. Mortality is less than 1%. 

Cirrhosis and other Uver diseases may result in the formation of excessive amounts of fluid in the abdomen ascites). The primary causes of ascites are usually elevation of pressure in the portal vein and a decreased amount of hepatic plasma protein production. Both factors tend to reduce the ability of the vascular compartment to retain fluid. The resultant ascites may contribute to decreased appetite and respiratory difficulties, among other symptoms. When these symptoms are present, careful reduction in the fluid volume through the use of diuretics is desirable. 

One of the major reasons for the popularity of the benzodiazepines is their relative safety. Overdoses with the benzodiazepines occur commonly, but fatal toxic occurrences are rare. Fatal intoxications are more likely in children, in individuals with respiratory difficulties, and in individuals who have consumed another central nervous system depressant, such as alcohol. After an overdose, the patient begins a deep sleep that may last for 24 to 48 hours, depending on the dose. However, even with large overdoses, the patient can usually still be aroused. 

Assess the patient for evidence of an allergic reaction, including hypotension, respiratory difficulty, and urticaria... 

Overdose may produce diarrhea, fast/irregular heartbeat, nausea continuing >30 min, stomach pain, respiratory difficulty, unusually tired, and aching/stiff muscles. 

Nervousness, change in sleep habits, headache, visual disturbances, paresthesia, diarrhea or constipation, palpitations, chest pain, rash, respiratory difficulty, edema... 

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